CCL2 and Sepsis: Our principal aims were as follows: (a) to evaluate whether endotoxin administration leads to increased MCP-1 expression in skeletal muscles; (b) to assess whether an increased exposure to MCP-1 has direct effects on skeletal muscle function; and (c) to determine whether MCP-1 neutralization is able to modulate proinflammatory mediator expression and contractile function in the diaphragm during acute endotoxemic sepsis.